There are a number of effects produced by inhomogeneous static magnetic fields like that of Q magnets, the main ones being increasing the pain threshold and dampening sensitized nerves. The following study looked at the effects on cell membrane stabilization.
OBJECTIVE: Swelling is a final common pathway to neuronal death following diverse insults that damage the central nervous system. Here we have tested the effect of a static magnetic field on neuronal edema induced by the excitotoxin, kainic acid (KA), in an effort to identify a new treatment strategy.
METHODS: Cultured mouse spinal cord neurons were superfused at 37°C with control buffer, buffer with altered ionic composition or buffer containing 125 m M kainic acid (KA) with/without different drugs (non-MAG). Different neurons were positioned in regions of a static magnetic field with steep variation of the field gradient produced by a square array of four permanent magnets of alternating polarity for 1-30 minutes prior (preRX ) to changing to the experimental superfusate (MAG). Digital image techniques, detection of changes in luminance through a selected neuron as a measure of cell swelling, and intracellular microelectrode recording techniques were used to assess cell size and function in different experimental solutions.
RESULTS: KA caused swelling and/or shrinking of neurons that commenced within 5 minutes of exposure with a peak mean increase in luminance (DL) of 22.5%. The rate and extent of swelling decreased after pretreatment with the magnetic field. A dose response relationship was observed on the basis of duration of pretreatment: 1 min. afforded no protection, 30 and 60 min afforded maximum protection (DL 5% and 7%, resp.), and 5 min exposure produced intermediate protection (DL 16%). After 30 min KA exposure and return to control solution for at least 1 hour, 34% of non-MAG and 40% of MAG neurons were penetrable with glass electrodes. These neurons had resting potentials and kainate responses similar to control neurons, but they only fired a few action potentials during a long depolarizing pulses, while firing of control neurons was sustained. The rest of non-MAG neurons appeared to disintegrate; the remaining MAG neurons still had intact cell bodies and processes but significant resting potentials could not be obtained on penetration with microelectrodes. Depolarization with 50 mM K+ did not induce neuronal swelling. Slight protection was afforded by tetrodotoxin (voltage-sensitive Na+ channel blocker). Reducing external Ca++ concentration provided little protection, alone or in combination with magnetic pretreatment. The KA antagonist CNQX limited swelling in concentration-dependent manner. The amplitude of KA responses was not reduced significantly by MAG preRX, but action potentials were blocked. Furosemide, an antagonist of the Na/Cl symporter, reduced swelling in concentration-dependent manner; MAG preRX enhanced protection. Magnetic field exposure after initiation of KA-induced swelling was ineffective.
SUMMARY AND CONCLUSIONS: Pretreatment with a static magnetic field reduced and slowed the rate of swelling induced by a high concentration of KA. This effect probably involved reduced entry of water and sodium and was mimicked by the diuretic furosemide. Other effects of KA were not blocked and neuronal death ensued after 30-60 min of exposure, probably due to entry and intracellular accumulation of calcium. Treatment with a gradient magnetic field may be a useful adjunct in the treatment of acute neuronal swelling.
A STATIC MAGNETIC FIELD SLOWS KAINIC ACID-INDUCED NEURONAL SWELLING.
M.J. McLean, R.R. Holcomb, P.W. Macdonald, L. Sanderson and K. Lombard. Department of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee 37212, USA.
Bioelectromagnetics Society Annual Meeting, June 20-24, 1999.
Long Beach, California, USA. 21st Annual Meeting
Entire proceedings can be downloaded at the following link…
This abstract is on page 35 of the document.
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